LIPOIC
ACID
Bibliography and References. Review.
List of selected scientific articles (abstracts). Experimental and clinical data..
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| Diabetes Obes Metab. 2005 May;7(3):294-7. BACKGROUND: Non-enzymatic glycation of proteins, leading to chemical
modification and cross-linking are of importance in the pathology of diabetic
complications. We studied the effect of alpha-lipoic acid (LA) on the
glycation and cross-linking of collagen from tail tendon of high-fructose-fed
rats. METHODS: The rats were divided into four groups of six each. Two
groups of rats were fed with a high-fructose diet (60/100 g diet) and
administered with either LA (35 mg/kg body weight, intraperitoneally)
(FRU + LA) or saline (FRU) for 45 days. The other two groups were fed
control diet containing starch (60/100 g diet) and administered with either
saline (CON) or LA (CON + LA). The rats were maintained for 45 days and
then sacrificed. Collagen was isolated from tail tendon and the extent
of glycation, fluorescence, aldehyde and peroxidation levels were measured.
The tail tendons were separated, and shrinkage temperature was also measured.
Acid-soluble collagen was extracted from tail tendon and subjected to
sodium dodecyl sulphate polyacrylamide gel electrophoresis. RESULTS: Fructose
administration caused accumulation of collagen in tail tendon. Glycation,
collagen-linked fluorescence, aldehyde and peroxide contents were elevated.
The gel pattern of acid-soluble collagen from the fructose-fed rat showed
elevated beta-component. These changes were alleviated by the simultaneous
administration of LA. CONCLUSION: Administration of LA has a positive
influence on tail tendon collagen glycation and other variables in high-fructose-fed
rats. Apoptosis. 2005 Mar;10(2):359-68. The antioxidant alpha-lipoic acid (ALA) has been shown to affect a variety
of biological processes associated with oxidative stress including cancer.
We determined in HT-29 human colon cancer cells whether ALA is able to
affect apoptosis, as an important parameter disregulated in tumour development.
Exposure of cells to ALA or its reduced form dihydrolipoic acid (DHLA)
for 24 h dose dependently increased caspase-3-like activity and was associated
with DNA-fragmentation. DHLA but not ALA was able to scavenge cytosolic
O(2) (-.) in HT-29 cells whereas both compounds increased O(2) (- .)-generation
inside mitochondria. Increased mitochondrial O(2) (- .)-production was
preceded by an increased influx of lactate or pyruvate into mitochondria
and resulted in the down-regulation of the anti-apoptotic protein bcl-X(L).
Mitochondrial O(2) (-.)-generation and apoptosis induced by ALA and DHLA
could be prevented by the O(2) (- .)-scavenger benzoquinone. Moreover,
when the lactate/pyruvate transporter was inhibited by 5-nitro-2-(3-phenylpropylamino)
benzoate, ALA- and DHLA-induced mitochondrial ROS-production and apoptosis
were blocked. In contrast to HT-29 cells, no apoptosis was observed in
non-transformed human colonocytes in response to ALA or DHLA addition.
In conclusion, our study provides evidence that ALA and DHLA can effectively
induce apoptosis in human colon cancer cells by a prooxidant mechanism
that is initiated by an increased uptake of oxidizable substrates into
mitochondria. Peptides. 2005 May 5; A quantitative autoradiographic study was performed to determine whether
kinin receptors are altered in the rat spinal cord in an experimental
model of arterial hypertension under antioxidant therapy with alpha-lipoic
acid. Sprague-Dawley rats were fed for 4 weeks with a normal chow diet
or with an alpha-lipoic acid supplemented diet (1000mg/kg feed), and treated
for the last 2 weeks with angiotensin II (AT II) (200ng/kg/min with an
osmotic pump implanted s.c.). Control rats received either diet but not
AT II. A 2-week administration of AT II increased significantly systolic
blood pressure, the production of superoxide anion in the aorta and B(1)
receptor binding sites in the thoracic spinal dorsal horn. This treatment
did not affect spinal B(2) receptor binding sites, glycemia and insulinemia.
The diet supplemented with alpha-lipoic acid reduced significantly the
increase in systolic blood pressure, the production of aortic superoxide
anion and prevented the increases of B(1) receptor binding sites. Results
show an association between the oxidative stress and the increases of
B(1) receptors and arterial blood pressure induced by AT II. Data also
exclude the possibility that arterial hypertension is a primary mechanism
leading to an increase of B(2) receptor binding sites in the rat spinal
cord. Mol Cell Biochem. 2005 Mar;271(1-2):133-8. PURPOSE: Ethanol exposure has been used to demonstrate the increase of
oxidative stress to a variety of tissues. We studied the effect of ethanol
on the response of isolated strips of rat bladder to in vitro hypoxia
in the absence of glucose (in vitro ischemia). Secondly, we determined
if alpha-lipoic acid (LA) could alter the response to ethanol + in vitro
ischemia. METHODS: Sixty-four rats were used for the these experiments.
Each rat was anesthetized and its urinary bladder excised. The bladder
body was cut into two longitudinal strips and each strip mounted in individual
baths filled with oxygenated Tyrodes solution containing glucose at 37
degrees C. Ethanol (0.3%, 1%, or 3%) was placed in the first six baths
(two strips at each concentration). The last two baths did not receive
ethanol. Each strip was incubated for 1 h and then stimulated with field
stimulation at 2, 8, and 32 Hz. Each strip was stimulated with 10 microM
carbachol, washed three times with fresh oxygenated buffer and ethanol
re-added to their respective baths. Each strip was then stimulated with
120 mM KCl and washed three times as before. Strips were then subjected
to 1 h in vitro ischemia (incubation in the absence of glucose with Tyrode's
equilibrated with nitrogen instead of oxygen). During the ischemic period,
each strip was stimulated for 5 s every 10 min by 32 Hz FS to simulate
hyperreflexia. At the end of the hour, the tissues were incubated for
an additional hour in the presence of oxygen + glucose and subjected to
a second series of stimulations as before. At all times, ethanol was maintained
in baths 1-6. In set 2, 1% ethanol was added to the first six baths. LA
was added to every other bath, and the experiments performed as mentioned
earlier. RESULTS: (a) Ethanol at 0.3% or 1% had no effect on the contractile
responses prior to exposure to in vitro ischemia; 3% was inhibitory. (b)
In vitro ischemia mediated a significant decrease in the contractile responses
to all forms of stimulation except for carbachol. (c) Ethanol mediated
a dose-response enhancement of the contractile dysfunctions caused by
in vitro ischemia. (d) LA completely reversed the effects of ethanol on
contractile responses following in vitro ischemia except for carbachol.
CONCLUSIONS: The results demonstrate that direct exposure to ethanol significantly
enhanced contractile dysfunctions mediated by in vitro ischemia followed
by re-oxygenation and that the presence of LA significantly inhibits this
effect of ethanol. J Clin Pharmacol. 2005 Mar;45(3):313-28. In an open-label, parallel-group study involving 16 patients (8 with
severely reduced renal function, 8 with end-stage renal disease needing
hemodialysis), the effect of renal function on the pharmacokinetics, metabolism,
and safety and of alpha-lipoic acid (thioctic acid) was evaluated by comparing
the pharmacokinetic parameters with those of a reference group of 8 healthy
subjects. Alpha-lipoic acid 600 mg was administered orally once daily
for 4 days, and the pharmacokinetic parameters were measured on days 1
and 4. The mean percentage of the administered dose excreted in urine
as parent compound was 0.2 and 0.05 in healthy subjects and subjects with
severely reduced renal function, respectively. Assuming a bioavailability
of 30%, this represents 0.67% and 0.17% of the bioavailable amount of
alpha-lipoic acid, respectively. The percentage of total urinary recovered
amounts of alpha-lipoic acid and 5 of its metabolites was 12.0 on both
days. The respective values for patients with severe kidney damage were
5.2% (day 1) and 6.4% (day 4). The total percentage of the administered
dose removed by hemodialysis was 4.0 in patients with end-stage renal
disease. Renal clearance of alpha-lipoic acid and its major metabolites,
6,8-bismethylthio-octanoic acid, 4,6-bismethylthio-hexanoic acid and 2,4-bismethylthio-butanoic
acid, were significantly decreased in subjects with kidney damage compared
to the reference group. Apparent total clearance of alpha-lipoic acid
was poorly correlated with creatinine clearance. There is strong evidence
that alpha-lipoic acid is mainly excreted by nonrenal mechanism or further
degraded to smaller units in the catabolic process. The significantly
increased area under the curve values of 4,6-bismethylthio-hexanoic acid
and half-lives of 2,4-bismethylthio-butanoic acid on both days in patients
with severely reduced function and end-stage renal disease were not considered
to be clinically relevant. Although trough levels of both metabolites
tend to increase slightly in these subjects, no accumulation effects were
detected. We conclude that the pharmacokinetics of alpha-lipoic acid are
not influenced by creatinine clearance and are unaffected in subjects
with severely reduced kidney function or end-stage renal disease. Hemodialysis
did not significantly contribute to the clearance of alpha-lipoic acid.
Hence, dose adjustment of alpha-lipoic acid is not necessary in patients
with renal dysfunction. Ophthalmologica. 2005 Jan-Feb;219(1):49-53. PURPOSE: The purpose of this study was to determine the protective effect
of alpha-lipoic acid against oxidative damage in rabbit conjunctiva and
cornea exposed to ultraviolet radiation. METHODS: 20 rabbits weighing
2,500- 3,000 g were used, and we divided them into 4 groups with 5 randomly
selected rabbits. The rabbits were exposed to 2 J/cm(2)/h of ultraviolet
A radiation (UVA) in the range of 320-405 nm for 12 h per day within 90
days. The control group did not undergo any procedure, the UVA group was
only exposed to UVA radiation. The PUVA group was treated with 8-methoxypsoralen
and UVA. The alpha-lipoic acid group was administered 8-methoxypsoralen
+ UVA + alpha-lipoic acid. At the end of 90 days, the rabbits were killed
by decapitation, and the eyes were enucleated. Both eyes of each rabbit
were used for biochemical evaluation. Conjunctival and corneal free malondialdehyde
(MDA), glutathione peroxidase (GSH-PX) and superoxide dismutase (SOD)
levels were compared among the groups. RESULTS: Conjunctival free MDA
levels were lower in the alpha-lipoic acid group compared with the UVA
and PUVA groups (p < 0.05, p < 0.001, respectively). Both conjunctival
SOD levels (p < 0.05, p < 0.01, respectively) and conjunctival GSH-PX
levels (p < 0.01, p < 0.001, respectively) were higher in the alpha-lipoic
acid group compared with other groups. Corneal free MDA levels were lower
in the alpha-lipoic acid group compared with the UVA and PUVA groups (p
< 0.01, p < 0.001, respectively). Both corneal SOD levels (p <
0.01, p < 0.01, respectively) and corneal GSH-PX levels (p < 0.01,
p < 0.01, respectively) were higher in the alpha-lipoic acid group
compared with the other groups. CONCLUSION: alpha-Lipoic acid which is
considered as potent antioxidant protects the eye from the damaging effect
of ultraviolet exposure. Copyright (c) 2005 S. Karger AG, Basel. Neurobiol Aging. 2005 Jun;26(6):899-905. Oxidative stress is associated with age-related declines of biological functions. However, the nervous system is preserved during aging in Caenorhabditis elegans and, thus, it is not well explored whether aging and oxidative stress affect nervous functions. Here we report that age-related decline can be observed in a type of associative-learning behavior, referred to as isothermal tracking. We also report the effects of mutants with altered sensitivity to oxidative stress on learning behavior and motor activity in young adults. The isp-1 and clk-1 mutants are members of the Clk class of mutants and have deficits in the function of the mitochondrial respiratory chain, leading to reduced levels of oxidative stress, increased longevity, delayed rhythmic behaviors and other phenotypes. Both the Clk mutations and pretreatment with a metabolic antioxidant, alpha-lipoic acid (LA), increased the ability to show isothermal tracking and modestly reduced motor activity. Mutants with increased oxidative stress showed severely impaired learning behavior and modestly reduced motor activity. Therefore, physiological levels of oxidative stress may be too high for learning behavior but, perhaps, not for motor activity. We discuss the relevance of oxidative stress to the aging and evolution of behaviors.
Several lines of evidence have suggested that triglyceride accumulation in skeletal muscle and pancreatic islets is causally related to type 2 diabetes mellitus. We recently showed that alpha-lipoic acid (ALA), a potent antioxidant and cofactor of mitochondrial respiratory enzymes, reduces body weight of rodents by suppressing food intake and increasing energy expenditure. We sought to determine if ALA can prevent the development of diabetes mellitus in obese Otsuka Long-Evans Tokushima Fatty (OLETF) rats. Most (78%) untreated OLETF rats showed glycosuria at 40 weeks of age, but this was completely prevented by ALA. Compared with untreated OLETF rats, ALA reduced body weight and protected pancreatic beta-cells from destruction. ALA also reduced triglyceride accumulation in skeletal muscle and pancreatic islets. These results indicate that ALA prevents diabetes mellitus in obese diabetes-prone rats by reducing lipid accumulation in non-adipose tissue as well as in adipose tissue. Expert Opin Investig Drugs. 2004 Dec;13(12):1641-3. Obesity shortens life expectancy and is a risk factor for hypertension and Type 2 diabetes. When added to the standard chow of Sprague-Dawley or Otsuka Long-Evans Tokushima Fatty rats, alpha-lipoic acid (0.5% weight/weight) reduced body weight and food intake. Alpha-lipoic acid also increased whole-body energy expenditure. It exerts its effects by suppressing hypothalamic AMP-activated protein kinase. Long-term studies to determine whether these anti-obesity effects are maintained in animals are required before alpha-lipoic acid is considered for clinical trial in human obesity. J Comp Physiol [B]. 2004 Nov;174(8):587-92. Epub 2004 Sep 29. Chronic feeding of fructose to normal rats causes impaired glucose tolerance,
loss of tissue sensitivity to insulin, hyperinsulinemia and hypertension.
alpha-Lipoic acid (LA), a co-enzyme known for its potent antioxidant effects,
stimulates insulin-mediated glucose uptake in clinical and experimental
diabetes. The purpose of this study was to examine whether LA can mitigate
fructose-induced insulin resistance and associated abnormalities. Male
Wistar rats of body weights 150-170 g were divided into 4 groups containing
12 rats each. Control rats received a control diet containing starch and
water ad libitum. Fructose rats received a fructose-enriched diet (>60%
of total calories). Fructose + LA rats received a fructose diet and LA
(35 mg/kg b.w.) intraperitoneally. Control + LA rats received a normal
diet and LA (35 mg/kg b.w.) intraperitoneally. After the treatment period
of 20 days, blood pressure (BP) was measured. Oral glucose-tolerance test,
insulin-sensitivity index, urea and creatinine clearance tests, and plasma
and urinary sodium and potassium levels were analysed. Kallikrein activity
and nitrite content were assayed. Additionally, the activities of RBC-membrane
Na(+)/K(+) ATPase and Ca(2+) ATPase enzymes were assayed. Fructose rats
showed increased BP, decreased glucose tolerance, decreased insulin sensitivity
and altered sodium and potassium levels and renal clearance. LA supplementation
mitigated these alterations. The increase in BP was attenuated and the
levels of biochemical parameters were brought close to normal. The BP-lowering
effect of LA in fructose rats may be related to improvement in insulin
sensitivity. Cell Biochem Funct. 2004 Nov 8. In the present study, we investigated whether DL-alpha-lipoic acid (LA) supplementation could have prooxidant or antioxidant effects on oxidative protein damage parameters such as protein carbonyl (PCO), nitrotyrosine (NT), advanced oxidation protein products (AOPP), and protein thiol (P-SH), as well as oxidative stress parameters such as total thiol (T-SH), non-protein thiol (Np-SH), and lipid hydroperoxide (LHP) in the brain and the skeletal muscle tissue of aged rats. PCO, and NT levels were increased, AOPP and P-SH levels were not changed in the brain tissue of aged rats given LA supplementation. On the other hand, TSH, Np-SH, and LHP levels were decreased in the brain tissue of aged rats given LA supplementation. The levels of the same parameters were not significantly different in the skeletal muscle tissue of aged rats given LA supplementation. The increased levels of protein oxidation markers such as PCO, and NT in the brain tissue of LA-supplemented aged rats compared with non-supplemented aged rats may suggest that oxidative protein damage is increased in LA-supplemented aged rats. We assume that an explanation for our findings regarding LA supplementation on protein oxidation markers in the brain tissue of aged rats may be due to the prooxidant effects of LA. Depending on post-mitotic tissue type and dosage of LA, the prooxidant effects of LA supplementation, should be considered in future studies.
AIM: to evaluate the effect of alpha-lipoic acid in autonomic diabetic
neuropathy in a controlled, randomized, open-label study. MATERIAL AND
METHODS: 46 patients with type 1 diabetes and different forms of autonomic
neuropathy, of mean age 38.1 +/- 12.5 years and mean duration of diabetes
16.8 +/- 8.9 years were treated with alpha-lipoic acid for 10 days 600mg
daily iv, thereafter one film tablet of 600mg daily for 50 days. 29 type
1 diabetic patients with autonomic diabetic neuropathy, of mean age 40.2
+/- 9.3 years and mean duration of diabetes 15.4 +/- 7.9 years served
as a control group. We have followed-up patients' complaints, Ewing's
tests, laboratory parameters of oxidative stress. RESULTS: There was a
significant improvement after treatment in the score for severity of cardiovascular
autonomic neuropathy--from 6.43 +/- 0.9 to 4.24 +/- 1.8 (p<0.001),
while in the control group it worsened from 6.18 +/- 1.3 to 6.52 +/- 0.9
(p>0.1). We found improvement in the Valsalva manoeuvre after treatment
- from 1.05 +/- 0.04 to 1.13 +/- 0.08 (p<0.001); in the deep-breathing
test -from 3.4 +/- 2.8 to 10.4 +/- 5.7 (p<0.001); and in the lying-to-standing
test--from 0.99 +/- 0.01 to 1.01 +/- 0.02 (p>0.1), while in the control
group there was no improvement. There was a beneficial effect of treatment
on the change of systolic blood pressure at the lying-to-standing test--from
22.7 +/- 11.5 to 9.8 +/- 7.9 (p<0.001), while in the control group
the change was 20.5 +/- 11.1 mmHg and 19.7 +/- 12.9 mmHg (p>0.1), respectively.
We found improvement in diabetic enteropathy in six patients; in the complaints
of dizziness, instability upon standing in six patients; in neuropathic
edema of the lower extremities in four patients and in erectile dysfunction
in four patients after treatment, while in the control group no change
was reported in the symptoms and signs of autonomic neuropathy by the
end of the follow-up period. There were changes in the laboratory parameters
of oxidative stress after therapy--total serum antioxidant capacity increased
from 20.42 +/- 1.8 to 22.96 +/- 2.3 microgH2O2/ml/min (p<0.05), serum
SOD activity - from 269.8 +/- 31.1 to 319.8 +/- 29.IU/l (p=0.02) and erythrocyte
SOD--from 0.89 +/- 0.10 to 1.11 +/- 0.09 U/gHb (p=0.04). CONCLUSION: Our
results demonstrate that alpha-lipoic acid (Thiogamma) appears to be an
effective drug in the treatment of the different forms of autonomic diabetic
neuropathy. Rom J Intern Med. 2004;42(2):293-9. Searching for more efficient treatments for diabetic neuropathy continues
to be a task for researchers and for practitioners also. The reasons are:
the poor quality of life and the risk for ulcerations/amputations induced
by peripheral diabetic neuropathy (PDP) (the most frequent manifestation
of diabetic neuropathy) and the risk for sudden death and other manifestations
attributed to autonomic neuropathy. There is a paucity of evidence based
interventions for PDP. In this situation, the recent evidence (randomized,
placebo controlled studies) regarding the efficacy of alpha-lipoic acid,
a powerful antioxidant, are bringing new hopes.
The heat shock response protects against sepsis-induced mortality, organ
injury, cardiovascular dysfunction, and apoptosis. Several inducers of
the heat shock response, such as hyperthermia, sodium arsenite, and pyrollidine
dithiocarbonate, inhibit NF-kappaB activation and nitric oxide formation.
The antioxidant lipoic acid (LA) has recently been found to inhibit NF-kappaB
activation and nitric oxide formation. We therefore tested the hypothesis
that LA induces a heat shock response. To test this hypothesis, we determined
whether exposure to LA affects expression of both heat shock protein 70
(HSP-70) and nuclear heat shock factor-1 (HSF-1) in lipopolysaccharide
(LPS) stimulated macrophages. LA and hyperthermia attenuated LPS-induced
increases in nuclear NF-kappaB, iNOS protein, and media nitrite concentrations.
LPS and hyperthermia increased HSP-70 concentrations 8-fold and 20-fold,
respectively. No effect of LA treatment alone on HSP-70 protein expression
was detected. Likewise, no effect of LA on HSF-1 protein expression was
detected. These data suggest that LA inhibits LPS-induced activation of
iNOS in macrophages independent of the heat shock response. Mol Cell Biochem. 2004 Jun;261(1-2):123-35. The mechanism of diabetic embryopathy is not known. Excessive reactive
oxygen species (ROS) produced in diabetes may be causally related to foetal
anomalies. The objective of this study was to determine whether supplementation
with the antioxidant lipoic acid (LA) could prevent maternal diabetes-related
foetal malformations and intrauterine growth retardation (IUGR) in rats.
Pregnant rats were non-treated (Group I) or made diabetic on gestation
day (GD) 2 by injecting streptozotocin (Group II). Group III was injected
with 20 mg kg(-1) of LA daily starting on GD 6 and continued through GD
19. Group IV was administered only Tris buffer on the corresponding days.
Group V was a set of STZ-treated animals, which were supplemented with
a daily dose of 20 mg kg(-1) of LA from GD 6 through GD 19. All fetuses
were collected on GD 20. Lipoic acid did not affect the blood sugar levels
of diabetic animals significantly but improved their body weight gain
and reduced food and water consumption. Diabetic group had a high incidence
of embryonic resorption, IUGR, craniofacial malformations, supernumerary
ribs and skeletal hypoplasia. Lipoic acid significantly reduced these
abnormalities. These data support the hypothesis that ROS are causally
related to fetal maldevelopment and IUGR associated with maternal diabetes
in the rat. They also highlight the possible role of antioxidants in the
normal processes of embryo survival, growth and development.
Alpha lipoic acid is a natural antioxidant that has been suggested to improve symptoms of diabetic neuropathy. To assess these potential benefits, a cohort of 26 type 2 diabetic patients with symptomatic peripheral neuropathy (stage 2) received a daily dose of 600 mg alpha-lipoic acid, and were followed for a 3 month-period. No dropout was noted. At the end of the follow-up period, in 20 subjects (76.9%) there was a 1-stage regression of somatic neuropathy (from symptomatic to asymptomatic neuropathy, and in 5 patients (19.2%) no signs of neuropathy were found. The nerve conduction velocity of motor fibers improved from 36.8 (95% Confidence Interval CI = 30.9-42.7) meters/second to 41.3 (95% CI = 39.5-43.0) meters/second (p = 0.049, paired t test). Mean blood glucose measured was significantly lower at 3 months than at baseline [197.9 (95% CI = 170.1-225.7) versus 162.2 (95% CI = 146.1-178.2 mg/dl, p = 0.02, paired t test)]. In a multiple linear regression model with age. sex, body mass index, diabetes duration and the difference between blood glucose values at 3 months and at baseline as explanatory variables, the increment in nerve conduction velocity was not accounted for by the improved glycemic control. Women, thinner and younger patients tended to benefit more from the treatment in terms of nervous conduction velocity improvement. In conclusion, alpha-lipoic acid seems to be efficient and safe in the treatment of diabetic peripheral neuropathy, improving both clinical manifestations and nerve conduction velocity. Placebo controlled clinical trials are needed to further define the role of this new medication in the treatment of diabetic neuropathies.
Arch Gerontol Geriatr. 1999 Aug;29(1):45-56. The well known OH? free radical scavenging properties of alpha-lipoic
acid (ALA) cannot be easily utilized for biological experiments, because
the compound is practically insoluble in water. We elaborated a simple
method of preparing its Na-salt (Na-ALA) which proved to be water soluble.
It has been demonstrated by ESR spin trapping experiments with DMPO, using
the Fenton reaction as the source of OH? free radicals that Na-ALA maintains
its OH? free radical scavenging ability: it reacts nearly an order of
magnitude faster with these radicals than the spin trap itself. It was
tested in two different systems to determine whether Na-ALA was able to
protect bovine serum albumin (BSA) against the OH? free radical-induced
polymerization and protein oxidation. (i) OH? free radicals were generated
by Fenton reaction in the presence of BSA. This protein is polymerized
by these radicals shown by the loss of its water solubility; Na-ALA exerted
a considerable protective effect against this type of protein damage.
(ii) BSA oxidation was induced by Co-gamma irradiation of 80 krad, resulting
in a strong increase in the protein carbonyl content. Na-ALA inhibited
this carbonyl formation very efficiently. The data suggest that the interaction
of the OH radical with Na-ALA takes place on the disulfide group, yielding
thiosulfinate or thiosulfonate. The results indicate that the geriatric
topical application of Na-ALA may have an established rationale.
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